Abstracts: ISEE 20th Annual Conference, Pasadena, California, October 12-16, 2008: Contributed Abstracts
PAHs are widespread ambient and indoor air combustion products from coal burning power plants, heating, cooking, and cigarette smoke. Previous work linked transplacental exposure to PAHs or PAH-DNA adducts_on the metabolic pathway of PAHs_to decrements in head circumference and birth weight, and impaired cognitive and motor development in childhood in our longitudinal cohort study in New York City (NYC). We also previously showed that prenatal exposure to PAHs significantly impairs fetal growth and the neurodevelopment of 6-month-old infants in an inner-city cohort study in Krakow (Poland), and suspect that subsequent neurodevelopmental outcomes will also be adversely affected in this highly exposed Caucasian cohort.
We explored the relationship between prenatal PAH exposure and the Mental Development Index (MDI) score (assessed using the Bayley Scales of Infant Development (BSID-II)).
Between November 2000 and December 2003, 505 non-smoking and otherwise healthy pregnant women were enrolled in Krakow. The participants provided demographic, health, and exposure information and carried air monitors for 48 hours in their second and/or third trimesters of pregnancy to report personal PAH exposure. We collected cord and maternal blood at delivery to measure cotinine (marker of exposure to environmental tobacco smoke (ETS)), PAH-DNA adduct levels, and plasma lead (Pb) concentrations, and assessed the development of the children at 1 year of age with MDI. Regression models included total PAHs ((ln) transformed continuous, or dichotomized as high/low), maternal education, and gender of newborns. We examined MDI both as the continuous score, and dichotomously (score <85 corresponding to moderate delay, vs. normal at ≥85). We restricted the analyses by quality of PAH monitoring data (QC < 3), and cotinine levels <25 ng/m3. Finally, we included lead (Pb), a known developmental toxicant and potentially important confounder, in our model.
We found a significant adverse effect of PAHs on MDI score at age 1 year (β = −1.03, P-value = 0.03). When dichotomizing MDI scores into delayed vs. non-delayed, the results were borderline significant. Including cord adducts in the model (neither cord nor maternal adduct levels alone were predictive of MDI at 1 year) did not change the effect size or significance of the association between PAH and MDI score at 1 year (β = −1.04, P-value = 0.04, n = 326), suggesting that the adverse effect of PAHs is not directly mediated by adducts, but by other mechanisms exerted by these pollutants. Including cord Pb in the model appeared to significantly confound the association between PAH exposure and MDI score.
This study shows that prenatal exposure to PAHs is detrimental to child neurodevelopment at age 1, and may be exerting its effect via a different mode of action than previously hypothesized. These results differ from NYC cohort results, where prenatal PAHs were not observed to affect neurodevelopment until the children were aged 3. Our findings also suggest that cord Pb may be the major pollutant affecting the health of children in this population.